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KROWY MLECZNE ZDROWIE I WYDAJNOŚĆ


Diagnosis:
The clinical diagnosis of ketosis is based on presence of risk factors (early lactation), clinical signs, and ketone bodies in urine or milk. When a diagnosis of ketosis is made, a thorough physical examination should be performed because frequently ketosis occurs concurrently with other peripartum diseases. Especially common concurrent diseases include displaced abomasum, retained fetal membranes, and metritis. Rabies and other CNS diseases are important differential diagnoses.
Cow-side tests for the presence of ketone bodies in urine or milk are critical for diagnosis. Caution should be exercised in the use of such tests within 48 hr after calving. Due to the large surge in plasma NEFA at calving, a positive test for ketones is very common during this period. The majority of commercially available test kits are based on the presence of acetoacetate or acetone in milk or urine. Dipstick tests are convenient, but those designed to detect acetoacetate or acetone in urine are not suitable for milk testing. All of these tests are read by observation for a particular color change. In a given animal, urine ketone body concentrations are always higher than milk ketone body concentrations. Trace to mildly positive results for the presence of ketone bodies in urine do not signify clinical ketosis. Without clinical signs, such as partial anorexia, these results indicate subclinical ketosis. Milk tests for acetone and acetoacetate are more specific than urine tests. Positive milk tests for acetoacetate and/or acetone usually indicate clinical ketosis. A dipstick designed to detect BHB in milk, available in Japan and Europe, is more sensitive than milk tests for acetone and acetoacetate and may be useful for monitoring incidence of subclinical ketosis.

Treatment:
Treatment is aimed at reestablishing normoglycemia and reducing serum ketone body concentrations. Bolus IV administration of 500 mL of 50% dextrose solution is a common therapy. This solution is very hyperosmotic and, if administered perivascularly, results in severe tissue swelling and irritation, so care should be taken to assure that it is given IV. Bolus glucose therapy generally results in rapid recovery, especially in cases occurring near peak lactation. However, the effect frequently is transient and relapses are common. Administration of glucocorticoids including dexamethasone or isoflupredone acetate at 5-20 mg/dose, IM, generally results in a more sustained response. Glucose and glucocorticoid therapy may be repeated daily as necessary. Propylene glycol (250-400 g/dose, PO, [~8-14 oz]) acts as a glucose precursor and may be effective as ketosis therapy, especially in mild cases or in combination with other therapies. This dose may be administered twice per day. Overdosing propylene glycol leads to CNS depression.
Ketosis cases occurring within the first 1-2 wk after calving frequently are more refractory to therapy than those cases occurring nearer to peak lactation. In these cases, a long-acting insulin preparation given IM at 150-200 IU/day may be beneficial. Insulin suppresses both adipose mobilization and ketogenesis, but should be given in combination with glucose or a glucocorticoid to prevent hypoglycemia. Use of insulin in this manner is an extra-label, unapproved use. Other therapies that may be of benefit in refractory ketosis cases are continuous IV glucose infusion and tube feeding. (See also fatty liver disease of cattle, Fatty Liver Disease of Cattle .)

Prevention and Control:
Prevention of ketosis is via nutritional management. Body condition should be managed in late lactation, when cows frequently become too fat. The dry period is generally too late to reduce body condition score. Reducing body condition in the dry period may even be counterproductive, resulting in excessive adipose mobilization prepartum. A critical area in ketosis prevention is maintaining and promoting feed intake. Cows tend to reduce feed consumption in the last 3 wk of gestation. Nutritional management should be aimed at minimizing this reduction. Controversy exists over the optimal dietary characteristics during this period. It is likely that optimal energy and fiber concentrations in rations for cows in the last 3 wk of gestation vary from farm to farm. Feed intake should be monitored and rations adjusted to maximize dry matter and energy consumption in late gestation. After calving, diets should promote rapid and sustained increases in feed and energy consumption. Rations should be relatively high in nonfiber carbohydrate concentration, but contain enough fiber to maintain rumen health and feed intake. Neutral-detergent fiber concentrations should usually be in the range of 28-30% with nonfiber carbohydrate concentrations in the range of 38-41%. Dietary particle size will influence the optimal proportions of carbohydrate fractions. Some feed additives, including niacin, calcium propionate, sodium propionate, propylene glycol, and rumen-protected choline, may be beneficial in preventing and managing ketosis. To be effective, these supplements should be fed in the last 2-3 wk of gestation, as well as during the period of ketosis susceptibility.


                                                                                                                                                   The Merck Veterinary Manual

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